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Related Concept Videos

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

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Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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Regulation of Angiogenesis and Blood Supply01:24

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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Cirrhosis II: Pathophysiology01:24

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Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to...
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Acute Inflammation II: Local and Systemic Effects01:25

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Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
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NF-κB-dependent Signaling Pathway02:26

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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
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Acute Inflammation I: Inflammatory Response01:26

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Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect...
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Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
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Hypoxia-sensitive pathways in inflammation-driven fibrosis.

Mario C Manresa1, Catherine Godson1, Cormac T Taylor2

  • 1School of Medicine and Medical Science and the Conway Institute, University College Dublin, Belfield, Dublin, Ireland.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|October 10, 2014
PubMed
Summary
This summary is machine-generated.

Tissue injury healing involves inflammation, proliferation, and resolution. Uncontrolled inflammation can cause fibrosis, a condition linked to hypoxia, impacting tissue repair and health.

Keywords:
NF-κBSmadfibrosishypoxiainflammation

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Area of Science:

  • Cellular and Molecular Medicine
  • Pathology
  • Physiology

Background:

  • Tissue injury triggers a conserved healing response with inflammatory, proliferative, and maturation phases.
  • Failure to resolve inflammation can lead to excessive scarring (fibrosis), a complication in diseases like Crohn's disease (CD).
  • Chronic inflammation alters tissue oxygen levels, causing localized hypoxia, which often coincides with fibrosis.

Purpose of the Study:

  • To review the cellular and molecular mechanisms of inflammation-driven fibrosis.
  • To explore the role of tissue hypoxia in the development of fibrosis.

Main Methods:

  • This is a review article, synthesizing existing research.
  • Focuses on cellular and molecular mechanisms.
  • Integrates findings on inflammation, fibrosis, and hypoxia.

Main Results:

  • Inflammation, fibrosis, and hypoxia are interconnected events in inflammation-driven fibrosis.
  • Current understanding of fibrosis mechanisms and therapeutic options is limited.

Conclusions:

  • Hypoxia may significantly influence the development of inflammation-driven fibrosis.
  • Further research into these mechanisms is crucial for developing new therapies.